best known of these reactions is the posttranslational hydroxylation of peptide-bound proline and lysine residues during formation of mature collagen. In these reactions, ascorbate is believed to reactivate the enzymes by reducing the metal sites of prolyl (iron) and lysyl (copper) hydroxylases (Englard and Seifter, 1986; Tsao, 1997).

Evidence also suggests that ascorbate plays a role in or influences collagen gene expression, cellular procollagen secretion, and the biosynthesis of other connective tissue components besides collagen, including elastin, fibronectin, proteoglycans, bone matrix, and elastin-associated fibrillin (Ronchetti et al., 1996). The primary physical symptoms of ascorbic acid's clinical deficiency disease, scurvy, which involves deterioration of elastic tissue, illustrate the important role of ascorbate in connective tissue synthesis.

Ascorbic acid is involved in the synthesis and modulation of some hormonal components of the nervous system. The vitamin is a co-factor for dopamine-β-hydroxylase, which catalyzes hydroxylation of the side chain of dopamine to form norepinephrine, and α-amidating monooxygenase enzymes, involved in the biosynthesis of neuropeptides. Other nervous system components modulated by ascorbate concentrations include neurotransmitter receptors, the function of glutamatergic and dopaminergic neurons, and synthesis of glial cells and myelin (Englard and Seifter, 1986; Katsuki, 1996).

Because of its ability to donate electrons, ascorbic acid is an effective antioxidant. The vitamin readily scavenges reactive oxygen species (ROS) and reactive nitrogen species (RNS) (e.g., hydroxyl, peroxyl, superoxide, peroxynitrite, and nitroxide radicals) as well as singlet oxygen and hypochlorite (Frei et al., 1989; Halliwell and Whiteman, 1997; Sies and Stahl, 1995). The one- and two-electron oxidation products of ascorbate are relatively nontoxic and easily regenerated by the ubiquitous reductants glutathione and NADH or NAD-PH. The relatively high tissue levels of ascorbate provide substantial antioxidant protection: in the eye, against photolytically generated free-radical damage; in neutrophils, against ROS produced during phagocytosis; and in semen, against oxidative damage to sperm deoxyribonucleic acid (DNA) (Delamere, 1996; Fraga et al., 1991; Levine et al., 1994). Ascorbic acid protects against plasma and low-density lipoprotein (LDL) oxidation by scavenging ROS in the aqueous phase before they initiate lipid peroxidation (Frei et al., 1988; Jialal et al., 1990) and possibly by sparing or regenerating vitamin E (Halpner et al., 1998). Evidence suggests that ascorbate

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